Pulse Field Ablation and SVT+AFib

I'm a male in early 40's with a long history of SVT. Ever since I was a teenager, I've experienced a random nightly pattern of falling asleep, only to open my eyes an hour later, wide awake as if I was never asleep. Shortly afterwards, a feeling of adrenaline rushes throughout my body and then my heart is off to the races. These episodes would last between 10-20min, depending on the intensity. Every time, I thought I was going to die.

All these years went by, and I was thought to have nocturnal panic disorder. I got really adept at waking up, coaching myself through the "panic attack", going back to sleep and living out my life. Even though I occasionally experienced episodes during waking hours, I was able to manage as best as I could.

In my 30's, something changed. Every once in awhile, I'd have a racing heart that degraded into something else -- something more scary. Each time this happened, I rushed myself to the ER but they could never catch anything. EKGs, Echocardiograms and Holter monitors turned up nothing. Since this was only happening once every few years, I convinced myself that I was simply having panic attacks with some extra palpitations on the side.

In late 2019, I woke up in the middle of the night, and immediately knew this was going to be an intense episode. I was riding it out at 165bpm, when I started to feel flutters in between the beats. It quickly degraded into an erratic tumble of rapid, disorganized soup, and I went into an all-out panic. I had my spouse call an ambulance, and when they hooked me up to an EKG, I was still at 150bpm -- they were convinced it was just SVT. After two unsuccessful injections of adenosine, they loaded me up and headed to the ER.

The 12 lead EKG in the ER revealed an immediate diagnosis: I was in AFib with RVR. I was transferred to the ICU, and it would be 14 hours and countless IV bags of potassium before I converted back to sinus rhythm. I was sent home with Metoprolol and Flecainide. However, I convinced my new cardiologist that we should hold off on Flecainide and just start with Metoprolol and see what happens.

Throughout 2020 and 2021, the AFib episodes started rolling in every few months. I tried everything, including a super strict diet and a well rounded exercise routine. Despite being in the best shape of my life, nothing could prevent the AFib episodes.

In January of this year, I agreed with my EP that it was time to try Flecainide. I was put on 50mg twice daily, and it was immediately life changing. I simply felt normal all the time, and the constant "anxiety" I was living with just disappeared. At that point it was obvious that my panic attacks were, in fact, SVT episodes. This was revelatory, and I was able to learn very quickly how a certain percentage of SVT patients develop AFib, just as I have.

The honeymoon was short lived -- after 5 months, last week I had my first episode of AFib while on Flecainide. Something also felt a bit different towards the end of the episode, so I landed in the ER again to make sure I wasn't going to drop dead of a new arrhythmia. They confirmed it was just AFib, and I self-converted in just under 3 hours.

The hope with Flecainide was that it could buy some time until Pulse Field Ablation was more mainstream. But this dark passenger is wrecking my life, and even though we could try upping the flec, I've had enough and I think it's time to get off the ride.

I'm in contact with Dr. Natale's team, and there is a new study "Admire" that is a single arm (i.e. every participant gets PFA). Because of my breakthrough AFib last week while on flec, I now qualify for the study.

My concern is that PFA in a study might be restricted to just PVI, rather than AVNRT and AVRT (where my AFib might be triggered via SVT).

Has anyone here had a similar experience with SVT leading to AFib? What drug combinations and/or procedures have you tried? Was anything successful?

The fact that adenosine didn't break the arrhythmia pretty reliably indicates it's not AVNRT or AVRT. With a rate hovering around 150 and adenosine being ineffective, atrial flutter is the more likely explanation (it's another form of SVT). I'm surprised no one ever made that diagnosis. It should be evident from the ECGs they obtained from your ER visits.

Since you're already in contact with Natale's people and you're an eligible candidate for the trial, I would go ahead with it without worrying about AVRT/AVNRT.

50mg flecainide is pretty low. Has anyone suggested 100mg twice a day? That is the maximum dosage if you weigh less than 154 pounds. If you weigh more than 154#, 300mg total in a 24 hour period is the maximum.

I was in nsr for 5 years straight on 100mg BID. Vomiting started a quick episode during year 5 and another 4 years later from chemo. So for 15.5 years I had those two episodes. Flecainide worked until it didn’t. After 15.5 years I lost a ton of weight and self experimented on 75mg BID. I had a breakthrough afib so I resumed the 100mg BID.

Get a flecainide serum lab test from labcorp. You get blood drawn exactly 11 hours after your last dose.

Until your ablation you may want to ask Natale’s team if you can increase the flecainide to 100mg twice a day to keep you in nsr. You may feel more comfortable. Worth a try to ask.

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Carey
The fact that adenosine didn't break the arrhythmia pretty reliably indicates it's not AVNRT or AVRT.

To my knowledge, Adenosine will slow, but not terminate, atrial fibrillation. Every episode of AFib that I've ever had starts as SVT and then degrades into AFib within 5-15min.

Even though the paramedics thought I was simply in SVT, they were incorrect because the RVR/150bpm was masking the situation. This is why Adenosine was ineffective. I personally knew it was different than SVT, which was confirmed in the ER to be AFib.

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susan.d
50mg flecainide is pretty low. Has anyone suggested 100mg twice a day? That is the maximum dosage if you weigh less than 154 pounds ... Get a flecainide serum lab test from labcorp

I am 198lbs and quite tall (slightly slim+athletic) so you are correct: 50mg twice daily is low, especially for my build. I am meeting with my EP tomorrow and plan to discuss 100mg twice a day and the flec serum lab test.

Wow, your situation sounds sounds just like mine. I’m on 50 mg of flecainide twice a day and lately I’ve been having PACs that scared the hell out of me. I told my EP at the Cleveland clinic I just can’t live like this any longer. I’m afraid to exercise and And I’m just waiting for the next episode. I may have to get Natale a call….

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tallguy31
Wow, your situation sounds sounds just like mine ... I just can’t live like this any longer. I’m afraid to exercise and And I’m just waiting for the next episode

I've followed your posts as a long time lurker, and definitely see the similarities in tall slim disposition and episode characteristics (middle of the night). Here's more detail about my situation, perhaps it can help with your fears of exercise:

Years back when I was significantly less predisposed to AFib, I was still dealing with SVT episodes (sometimes multiple times per week). At the time I was quite fit, lifting weights and constant cardio so I was careless about my diet. GERD was an issue since late 20's, and I noticed a correlation with big meals late at night as a trigger for SVT. Also, high pressure situations of sudden exercise could trigger these episodes too. I stopped eating so late at night, and avoided huge dinners filled with excessive carbs/fat/salt. I'd also try my best to sufficiently warm up slowly before high intensity exercise or sports.

As I mentioned previously, my situation has deteriorated in the past few years, with all my patterns/tricks/techniques proving less effective. In fact, before flecainide it had gotten so bad that any physical activity after dinner (going upstairs, taking out the trash) could be a trigger for an SVT episode. The food correlation is there, but unfortunately feels like matrix theory in definitively pinning down a smoking gun. Recently I read The AFib Cure by John D. Day and it helped immensely to improve my diet, especially around simple carbs and added sugars. My GERD has been virtually eliminated, but it feels too little too late as my cardiac tissue has likely been sufficiently remodeled for AFib, given the frequency of my episodes.

What I've discovered is that morning exercise (via rowing machine) is my last refuge; a safe space. Before any food or coffee, I take the first dose of flec and I can hit the rower uninhibited without fear of palpitations, SVT, etc. Each meal that I eat throughout the day increases my predisposition for SVT triggered by activity, but morning exercising will actually reduce the racy-heart effect of subsequent meals.

This study helped me better understand my particular situation, especially the interaction between SVT and AFib: [academic.oup.com]

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susan.d
50mg flecainide is pretty low. Has anyone suggested 100mg twice a day? That is the maximum dosage if you weigh less than 154 pounds. If you weigh more than 154#, 300mg total in a 24 hour period is the maximum

. Do you have a reference for the weight recommendations on Flecainide? I had one EP who didn’t seem to think weight was a factor in dosing, so it would help to have a reference—thanks.

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rel
To my knowledge, Adenosine will slow, but not terminate, atrial fibrillation. Every episode of AFib that I've ever had starts as SVT and then degrades into AFib within 5-15min.

Sure, that's entirely possible, but my point was that the lack of response to adenosine rules out AVRT/AVNRT. What you're left with as possible culprits are afib, flutter, and atrial tach. I think flutter is by far the most likely culprit. But even if AVRT/AVNRT are the actual culprits that initiate your afib, the fact that they're able to do so means the afib is there and has to be addressed on its own. Once it's out of the way AVRT/AVNRT should be fairly easy to identify, hopefully in the same procedure.

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Carey
But even if AVRT/AVNRT are the actual culprits that initiate your afib, the fact that they're able to do so means the afib is there and has to be addressed on its own. Once it's out of the way AVRT/AVNRT should be fairly easy to identify, hopefully in the same procedure.

I originally followed the same logic of ablating both sources in one procedure, but unfortunately this study yielded counterintuitive results: [academic.oup.com]

In a nutshell, they split SVT patients into three groups, ablations addressing 1.) SVT sources only 2.) Both SVT and AFib sources 3.) AFib only

Surprisingly, the ones ablated for just SVT had the best outcomes. I will ask both Dr Natale and my primary EP and see if they have any further insights.

By all means do ask them because that's a 12-year old article and the ablation landscape was vastly different then. Also, they completely ignored flutter, which is the most likely form of SVT to accompany afib. All in all, I don't think I would put a lot of importance on that one study as it pertains to you now in 2022. I don't think it's all that relevant to you.

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Carey
they completely ignored flutter, which is the most likely form of SVT to accompany afib

Worth sharing is that I'm acutely aware of every arrhythmia or palpitation I experience, as well as the differences between them all. I know when I'm having isolated PVCs vs PACs. I know pure SVT like the back of my hand, with hundreds of episodes in my lifetime. One ER visit even caught and diagnosed SVT, this was before AFib made a grand 14 hour entrance.

When I'm in SVT, I can feel the PACs start. I know when the PACs degrade to atrial flutter, and I know exactly when the atrial flutter degrades into AFib. There's even been a few isolated incidents where I got to flutter but then quieted down back to NSR, without progressing into AFib. One such episode was recorded on the Zio patch which confirmed that I knew the difference. Sometimes, on my way back from AFib to NSR, I'll have PVCs in bigeminy or trigeminy pattern. I can feel all the nuances.

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Carey
don't ... put a lot of importance on that one study as it pertains to you now in 2022

The reason it's important is because there's very little information to be found on my unique situation. Half a dozen cardiologists over 20 years failed at properly diagnosing me -- who knows where I'd be if the SVT episodes were properly managed before AFib took residence? What if I only experienced ~100 episodes of SVT instead of ~500 in my lifetime? How much more time without AFib would that have bought me?

I don't take ablation lightly. If we don't account for SVT and that results in an unsuccessful outcome, I would be devastated. On the other hand, if restrictions within this study prevent Dr Natale from addressing AVRT/AVNRT, I have to find a way to hold out until PFA usage is more widely available. The road feels narrow.

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Daisy

50mg flecainide is pretty low. Has anyone suggested 100mg twice a day? That is the maximum dosage if you weigh less than 154 pounds. If you weigh more than 154#, 300mg total in a 24 hour period is the maximum
. Do you have a reference for the weight recommendations on Flecainide? I had one EP who didn’t seem to think weight was a factor in dosing, so it would help to have a reference—thanks.

Read Anti-fib and George’s links
[www.afibbers.org]

Weight does make a difference. I had a flecainide overdose and my hr remained in 24 hr for days in the ICU. Flecainide is not a drug one experiments with. Read my links too.

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susan.d
Weight does make a difference. I had a flecainide overdose and my hr remained in 24 hr for days in the ICU. Flecainide is not a drug one experiments with. Read my links too

Thanks. I read the thread and all the links, very helpful. I have no doubt about the potential toxicity of flecainide as it caused complete heart block for me. However, I did not see a reference to the weight limitations for dosing in the links, which would be helpful to show to doubting cardiologists.

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Daisy

Weight does make a difference. I had a flecainide overdose and my hr remained in 24 hr for days in the ICU. Flecainide is not a drug one experiments with. Read my links too
Thanks. I read the thread and all the links, very helpful. I have no doubt about the potential toxicity of flecainide as it caused complete heart block for me. However, I did not see a reference to the weight limitations for dosing in the links, which would be helpful to show to doubting cardiologists.

Hope this is helpful:
[pubmed.ncbi.nlm.nih.gov]

“The dose was 300 mg for patients >70 kg, 200 mg for patients 40 to 70 kg, and 5 mg/kg for patients <40 kg.”

It’s a study for kids based on weight.

“



Edited 1 time(s). Last edit at 06/08/2022 02:47PM by susan.d.

Quick update, I saw my EP today and we have agreed to double the flec to 100mg twice daily.

In talking more deeply surrounding my situation, my EP raised the possibility of "Concealed" WPW as a potential cause my early onset AFib. This presents a conundrum, because with normal WPW, it would be an obvious decision to move forward with an ablation. Unfortunately with Concealed WPW, there's no reliable, non-invasive way to discover its existence. He said that 95% of his SVT ablations are AVNRT/AVRT, but the remaining 5% reveals Concealed WPW as a discovery during the procedure.

Regardless, the course of action remains the same: upping the flec and hoping it buys me a few years until PFA is more widely available. If the adjustment proves ineffective, there's now one more reason to take the plunge with an ablation. But I still have to talk with Dr. Natale about the flexibility of PFA during this study, especially if any of WPW/AVRT/AVNRT turns out to be a major factor.

[emedicine.medscape.com]

“ The two main treatment approaches to WPW syndrome are (1) pharmacotherapy and (2) EPS with RF catheter ablation. EPS with ablation is the first-line treatment for symptomatic WPW syndrome and for patients with high-risk occupations. It has replaced surgical treatment and most drug treatments. RF ablation used in conjunction with cryoablation for septal APs and APs near small coronary arteries has had high success rates with low risk. [17]
Drug therapy can be useful in some instances, such as in patients who refuse RF ablation and in temporizing patients with a higher risk of ablation-related complications (eg, AV block with pacing requirement for anteroseptal or midseptal pathways). Medical therapy may also be appropriate in pregnant women until radiation exposure is safe.
In choosing drug therapy, keep in mind that class Ic and class III antiarrhythmic medications will slow AP conduction, facilitating blockage of SVT. If the patient has a history of AF or atrial flutter, an AV nodal blocking medication should also be used.”

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susan.d
keep in mind that class Ic and class III antiarrhythmic medications will slow AP conduction, facilitating blockage of SVT. If the patient has a history of AF or atrial flutter, an AV nodal blocking medication should also be used.”

Thanks for the reference @susan.d — if I’m interpreting this correctly, flec+metoprolol combo is inline with current pharma recommendations in the case of WPW?



Edited 1 time(s). Last edit at 06/09/2022 03:10AM by rel.

After a day of researching WPW with AFib, I have significant concerns. Degradation to Vfib is a very real risk, and that’d be game over: SCD. However, I did read this:

“Patients with concealed WPW syndrome are not at risk [of Vfib] because in them, antegrade conduction does not occur over the accessory connection.”
[www.merckmanuals.com]

The uncertainty of potentially having WPW is unnerving. I cannot live life with SCD in the back of my mind.

Most of my knowledge of WPW is from a friend who has it and had a WPW ablation in maybe 2008. She got the ablation because of the Vfib risk, as she spends a fair amount of time in remote areas where help would be a long time in coming. She's also a volunteer ski patroller, so knows the risks well. In her case, the WPW is genetic, as her mother had it also. I do know that a WPW ablation seems to require a lower skill level than an afib ablation - kill the extra pathway(s). In your case, it would seem wise to fix afib, flutter and potential WPW all at the same time.

Most that I know with WPW have the SVT present during exercise.

In my ablated friend's case, even with the successful ablation, she still has weird rhythms. It is very easy for her heart to accelerate to high rates with little exertion. In her case, a high carb diet seems to accentuate this issue. Also, copious Zone 2 training seems to ameliorate this acceleration.

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GeorgeN
is very easy for her heart to accelerate to high rates with little exertion. In her case, a high carb diet seems to accentuate this issue. Also, copious Zone 2 training seems to ameliorate this acceleration.

Wow George, this is a dead ringer for for me, thanks for sharing. High carbs (especially at dinner) puts me in the danger zone, and very little exertion while in this zone can trigger an episode. And of course there’s no exertion in the case where I wake up to an episode shortly after falling asleep. My theory is that sudden, outsized blood sugar fluctuations cause an endocrine response, and a particular combination of chemicals that are released will activate errant cardiac pathways. Then we’re off to the races. I’m interested in trying the Freestyle Libre 3 continuous patch to test this blood sugar theory.

I also relate to the benefits of zone 2 training. It has always reduced the frequency of episodes, and unfortunately over the years I’ve been way less consistent with exercise than 20’s + early 30’s.

I have to circle back with my EP to really zero in and quantify the VFib risk in the event I do have Concealed WPW + AFib. In the meantime, I’m back to a diet with zero simple carbs/added sugars and exercising daily with the rowing machine.

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rel

is very easy for her heart to accelerate to high rates with little exertion. In her case, a high carb diet seems to accentuate this issue. Also, copious Zone 2 training seems to ameliorate this acceleration.

Wow George, this is a dead ringer for for me, thanks for sharing. High carbs (especially at dinner) puts me in the danger zone, and very little exertion while in this zone can trigger an episode. And of course there’s no exertion in the case where I wake up to an episode shortly after falling asleep. My theory is that sudden, outsized blood sugar fluctuations cause an endocrine response, and a particular combination of chemicals that are released will activate errant cardiac pathways. Then we’re off to the races. I’m interested in trying the Freestyle Libre 3 continuous patch to test this blood sugar theory.

I also relate to the benefits of zone 2 training. It has always reduced the frequency of episodes, and unfortunately over the years I’ve been way less consistent with exercise than 20’s + early 30’s.

I have to circle back with my EP to really zero in and quantify the VFib risk in the event I do have Concealed WPW + AFib. In the meantime, I’m back to a diet with zero simple carbs/added sugars and exercising daily with the rowing machine.

If a doc won't prescribe a Libre, you can purchase a pair here for $150 US [www.mycshonline.com] This may be the older version (I've used this version, never the newer one). This version will work without a meter if you have an iPhone 7 or better. I don't know the Android specs (I've got a 6s and use a meter). Dr. Mark Cucuzzella is a friend and did a presentation on the Libre here [www.youtube.com] One thing to note is to ignore 1st 24 hours of data, they are trash. Everyone knows this.

If I have blood sugar an hour after a meal (especially dinner) > 100 mg/dL, I will do 15-20 minutes of Zone 2 and it will usually drop it into the low 80's or high 70's. Doing this before bed sets me up for a nice morning glucose typically in the low 80's.